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1 Division of Nephrology and Hypertension and the Center for Hypertension and Renal Disease Research, Georgetown University Medical Center, Washington, DC, USA
* To whom correspondence should be addressed. E-mail: wilcoxch{at}georgetown.edu.
Oxidative stress accompanies Ang II infusion, but the role of AT1 vs. AT2 receptors (R) is unknown. Methods: We infused Ang II subcutaneously in rats for one week. Excretion of 8-IsoPGF2
(8-Iso) and malonyldialdehyde (MDA) were related to renal cortical mRNA abundance for subunits of NADPH oxidase and superoxide dismutases (SODs) using real time PCR. Subsets of Ang II-infused rats were given the AT1-R antagonist, candesartan (Cand) or the AT2-R antagonist, PD-123,319 (PD). Results: Compared to vehicle (Veh), Ang II increased 8-Iso excretion by 41% (Veh: 5.4 ± 0.8 vs. Ang II: 7.6 ± 0.5 pg[[rad]]24h-1; p<0.05). This was prevented by Cand (5.6 ± 0.5; p < 0.05) and increased by PD (15.8 ± 2.0; p < 0.005). There were similar changes in MDA excretion. Compared to Veh, Ang II significantly (p < 0.005) increased the renal cortical mRNA expression of p22phox (2-fold), Nox-1 (2.6-fold) and Mn-SOD (1.5-fold) and decreased Nox-4 (2.1-fold) and EC-SOD (2.1-fold). Cand prevented all these changes except for the increase in Mn-SOD. PD accentuated changes in p22phox and Nox-1 and increased p67phox. Conclusion: Ang II infusion stimulates oxidative stress via AT1-R, which increases the renal cortical mRNA expression of p22phox and Nox-1 and reduces abundance of Nox-4 and EC-SOD. This is offset by strong protective effects of AT2-R, which are accompanied by decreased expression of p22phox , Nox-1, and p67phox.
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